ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by van den Dungen, J. J.
Right arrow Articles by Wildevuur, C. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by van den Dungen, J. J.
Right arrow Articles by Wildevuur, C. R.

The Annals of Thoracic Surgery, Vol 35, 406-414, Copyright © 1983 by The Society of Thoracic Surgeons


ARTICLES

The effect of prostaglandin E1 in patients undergoing clinical cardiopulmonary bypass

JJ van den Dungen, GF Karliczek, U Brenken, JN van der Heide and CR Wildevuur

The effect of prostaglandin E1 (PGE1) on protection of platelets during cardiopulmonary bypass (CPB) was evaluated in 9 patients, who were compared with an identical control group of 10 patients undergoing coronary artery bypass grafting. To evaluate the hemodynamic side- effects, PGE1 (0.05 micrograms/kg/min) was infused prior to CPB, resulting in a 26% drop in mean systemic arterial pressure. With this dose, no inhibition of the adenosine diphosphate-induced aggregation could be measured in the pulmonary artery sample. During CPB, the same infusion dose resulted in a severe drop in systemic arterial pressure below 50 mm Hg in 7 of the 9 patients. In 5 of these patients, volume load and phenylephrine infusion could not compensate for the pressure drop, and PGE1 had to be reduced to 0.02 micrograms/kg/min. Platelet aggregation was reduced significantly in the PGE1-treated group compared with the control group, but not completely inhibited during CPB. However, in the postbypass period no platelet preservation was seen in the PGE1 group. In both groups, platelet number and function were equally low. No differences were measured in blood loss or blood transfusion requirements. Except for hypotension, no side-effects of the PGE1 treatment were seen. It is concluded that the hypotension caused by minimal doses of PGE1 during CPB precluded using higher doses, which might have had a greater effect on platelet inhibition. These hypotensive side-effects should be reduced or eliminated before PGE1 can be expected to have the same protective effect on platelet damage that has been demonstrated in animal experiments.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS
Copyright © 1983 by The Society of Thoracic Surgeons.